THE BEREITSCHAFTSPOTENTIAL, L-DOPA AND PARKINSONS-DISEASE
THE BEREITSCHAFTSPOTENTIAL, L-DOPA AND PARKINSONS-DISEASE
复制标题
DOI：
10.1016/0013-4694(87)90075-7
复制
发表时间：
1987-03-01
期刊：
影响因子：
--
通讯作者：
MARSDEN, CD
中科院分区：
文献类型：
--
作者：
DICK, JPR;CANTELLO, R;MARSDEN, CD
研究了正常人和帕金森病患者食指伸展运动前的Bereitschaftspotentials（BP）。在这两种情况下，研究了L-DOPA治疗前后的BP，此外，正常受试者在多巴胺拮抗剂后进行了研究。在患者和正常受试者中，L-DOPA引起BP早期部分和峰值负性点的振幅增加，就在EMG开始之前（N1），但它没有引起BP晚期偏侧部分的增加（NS“of Shibasaki）：在正常受试者中，多巴胺能拮抗剂引起N1振幅降低。对照实验表明，L-DOPA引起的变化并不是关闭药物时运动较慢或触发不良的结果。对帕金森病患者，左旋多巴治疗后的峰值血压负波（N1）的变化与其临床活动度的变化无相关性，此外，尽管帕金森病患者的早期血压振幅略有下降，但OFF治疗的患者的峰值血压负波与年龄匹配的正常人的峰值血压负波无差异;这是通过左旋多巴治疗扩大的同一部分。这些发现表明N1不受帕金森病的影响，多巴胺能药物对N1的作用是通过对纹状体以外其他部位多巴胺能机制的作用介导的，可能是在大脑皮层本身。左旋多巴的作用将需要在帕金森病的BP后续研究中考虑在内。
Bereitschaftspotentials (BPs) prior to extension movements of the index finger were studied in normal subjects and in patients with Parkinson''s disease. In both, BPs were studied before and after L-DOPA therapy, in addition, the normal subjects were studied after dopamine antagonists. In both patients and normal subjects, L-DOPA caused an increase in the amplitude of the early part of the BP and of the point of peak negativity, just prior to EMG onset (N1) but it did not cause an increase of the late lateralized part of the BP (NS'' of Shibasaki): in normal subjects dopaminergic antagonists caused a decrease in the amplitude of the N1. Control experiments suggested that the change caused by L-DOPA was not the result of slower movement or poorer triggering when OFF drugs. For patients with Parkinson''s disease there was no correlation between the change in their peak BP negativity (N1) after L-DOPA and their change in clinical mobility; in addition, there was no difference in the peak BP negativity of patients OFF therapy and that of age-matched normals, though there was a slight decrease in the amplitude of the early part of the BP for the patients with Parkinson''s disease; this was the same part that had been enlarged by L-DOPA therapy. These findings suggest that the N1 is not affected by Parkinson''s disease and that the effect of dopaminergic drugs on the N1 is mediated by actions on dopaminergic mechanisms elsewhere than in the striatum, perhaps in the cerebral cortex itself. The effect of L-DOPA will need to be taken into account in subsequent studies of the BP in Parkinson''s disease.